ISLETMESENCHYME Berichtzusammenfassung

Glucose homeostasis relies on the tightly controlled release of insulin by pancreatic beta-cells. Diabetes, characterized by increased blood glucose levels, is a chronic disease that is now reaching epidemic proportions. The most common form of this disease is Type 2 diabetes (T2D), which was previously regarded as a disease of insulin resistance. However, work over the past decade has shifted this paradigm by implicating beta -cell failure as a key factor in T2D. Despite major progress, the cellular and molecular basis of T2D is far from being elucidated. Here, we characterize islet-associated mesenchymal cells (isMCs), which have close contact with beta-cells in both human and mouse pancreata. Our preliminary findings revealed that isMCs function to maintain beta-cell maturity and function. Next, we linked genes associated with T2D in human to isMC function. Our preliminary results indicate that T2D-related changes in isMCs leads to impaired beta-cells mass and function, resulting in abnormal glucose regulation. Finally, we found disease-related changes in isMCs gene expression. Our findings point to isMCs as new players in glucose regulation. Furthermore, our results to date suggest that pathological changes in the islets niche contribute to beta-cell dysfunction and diabetes.